The purpose of this research was to investigate mechanisms underlying sodium deprivation-induced changes in peripheral gustatory neural responses to salt taste stimulation of the tongue. Previous studies have shown a strong link between increased NaCl intake and reduced chorda tympani nerve (CT) responses to NaCl stimulation of lingual taste receptors after dietary sodium deprivation in rats. Recent studies from our laboratory showed that 48 hours of dietary Na+ deprivation resulted in an increase in rats’ licking responses to concentrated NaCl solutions and a reduction in their CT responses to NaCl. Furthermore, amiloride, a pharmacological antagonist of epithelial sodium channels (ENaC), suppressed CT responses to NaCl in control rats, but had virtually no effect on CT responses to NaCl in Na+-deprived rats. Na+ deprivation also activates the renin-angiotensin system and adrenal aldosterone release after just 24-h, resulting in sodium conservation through reduced urinary Na+ output. We hypothesized that the increase in aldosterone was causally related to changes in CT responses to NaCl following sodium deprivation.
The first experiments determined the time when Na+-deprived rats first showed increased behavioral responses and reduced neural responses to NaCl. The results showed that at least 24-48 h of sodium deprivation was necessary. In addition, amiloride suppression of CT responses to NaCl was reduced in Na+-deprived animals indicating the involvement of ENaC. We also examined the role of aldosterone in peripheral gustatory signaling following dietary Na+ deprivation. Serum aldosterone levels were positively correlated with intake of a concentrated NaCl solution. Surprisingly, although serum aldosterone levels increase after 24-h of dietary Na+ deprivation, there was no effect of aldosterone blockade on CT responses to NaCl. In this experiment, 48-h of dietary Na+ deprivation did not reduce CT responses to NaCl. We investigated the effects of artificial saliva and dH2O rinse solutions on CT responsiveness following dietary Na+ deprivation. In this experiment, we found that 48-h of dietary Na+ deprivation reduced CT responses to NaCl when either artificial saliva or dH2O served as the rinse. Furthermore, independent of dietary Na+ state, amiloride suppression of CT responses to NaCl was greater when artificial saliva was the rinse solution. Finally, we hypothesized that intragastric infusion of a NaCl load equivalent to the amount ingested in behavioral studies may restore CT nerve responsiveness of Na+-deprived rats. Unfortunately, we were unable to complete this study as we did not observe a reduction in CT responses following dietary Na+ deprivation. However, CT responses in both groups were significantly greater following the infusion, suggesting that an intragastric infusion of NaCl may have the ability to alter taste responses to NaCl.
Together these studies provide insight into mechanisms underlying the changes in peripheral gustatory responses following dietary Na+ deprivation. Short-term Na+ deprivation reduced CT responses to NaCl, but the effect seems weak, as it was not always reproducible. Nevertheless, aldosterone may act along with other hormonal mechanisms to alter peripheral taste responses that may be necessary for increased NaCl intake following dietary Na+ deprivation.
